We tend to think of pre-eclampsia as this dangerous yet somewhat nebulous hypertensive disorder in pregnancy that = OB consult, delivery. But what is the pathophysiology behind pre-eclampsia? And why the heck does it place one at risk for eclampsia?
[spacer height=”20px”]1. Brief Pathophys, because it’s interesting! (Warning: the word trophoblast will make an appearance)
[spacer height=”20px”]Important: Pre-eclampsia = placentally mediated, aka its cause has nothing to do with the fetus.
[spacer height=”20px”]Now then: In a normal pregnancy, trophoblastic cells invade the endothelium and tunica media of the spiral arteries throughout the first 20 weeks, to enable remodeling of these arteries to form large tortuous vessels providing copious blood flow to the placenta/fetus. In pre-eclampsia, there is a failure of this trophoblastic migration, ultimately preventing the remodeling of the spiral arteries so that they remain these puny, narrow vessels leading to hypoperfusion of the placenta. Injury and ischemia occur causing the release of vascular mediators and consequent endothelial dysfunction in the form of increased tone, as well as increased vascular permeability. As such, these patients are actually intravascularly depleted, hypertensive and edematous. No bueno. Gentle hydration is recommended due to rapid third spacing (although, really only one study and pretty imperfect). The one known fix is delivery of this damaged placenta ASAP.
[spacer height=”20px”]2. Why eclampsia?
[spacer height=”20px”]The aforementioned endothelial dysfunction extends to target organs like the brain, liver, kidneys and right back to the placenta. Multiple studies have demonstrated the efficacy of magnesium over other anticonvulsants in the treatment of eclampsia perhaps due to its smooth muscle relaxant effect.
[spacer height=”20px”] Re: Photo – Poor Lady Sybil died from complications of eclampsia. Heartbreaking episode!
Image taken from: www.flickr.com